There are a wide variety of brain disorders which impair ability to perform posture and motor acts such as standing, walking, and manipulating objects. Examples of such brain disorders include: cerebellar degeneration, Parkinson's disease, traumatic brain injury, multiple sclerosis, and age-related degenerative disorders (see for example Kendal and Schwartz, 1981). Stroke and traumatic head injury can also impair posture and movement controls. And, cerebral palsy and certain forms of developmental learning disorders impair these motor functions. In all of the above instances, the nature and extent of impairment can vary widely, depending on the localization and extent of the brain injury. It is common, for example, that impairment is distributed unequally on the two sides of the body. Within a given body or limb part, muscles exerting force in one direction can be affected differently than those working in the opposite direction. In other instances, impairment can be unequally distributed between sensory and motor aspects of posture and movement control.
Nervous system disorders which impair the brain centers and associated efferent neural pathways controlling activities of the body musculature affect the motor components of posture and equilibrium control. Disorders of this type can result in partial or complete paralysis, or an inability to adequately contract muscles. Muscle paralysis can take the form of one or a combination of slow, weak, or fatiguable contractions, and can be localized to small groups of muscles or widely distributed (see for example Kendal and Schwartz, 1981; Chapters 27 through 29). Alternatively, impairment of brain centers controlling the activities of muscles can result in dyscoordination, contraction of inappropriate muscles or of appropriate muscles in inappropriate timing sequences (Nashner, et al, 1983). In the case of equilibrium control, disorders of postural movement control impair a subject's ability to execute coordinated movements back to an equilibrium position following perturbations therefrom.
Disruption of the brain centers and associated afferent neural pathways from peripheral receptors and muscles, in contrast, disrupts ability to receive and correctly interpret incoming somatosensory information used by the brain to sense muscle forces, joint positions, and orientations of body parts in relation to supporting surfaces. Disorders of this type can result in weak, inappropriate, and inaccurate postural movements and in an inability to maintain an equilibrium position (see for example Kendal and Schwartz, 1981; Chapters 24, 27, and 28).
Presently available clinical methods do not selectively assess both the type and the distribution of sensory and motor disorders impairmenting posture and equilibrium control:                (1) deep tendon reflexes: Briskly striking the tendon of a muscle produces a brief stretch input exciting stretch receptor organs and, by way of spinal pathways, motor units of the perturbed muscle. Since muscles isolated from central brain efferent controls tend to be overly responsive to brief stretch inputs, physicians use this test to determine the distribution of brain lesions. Deep tendon reflexes, however, do not selectively assess the sensory and motor components of the central brain lesion. Nor are they useful in understanding the functional problems of the patient or predicting the outcome of therapy (Holt, 1966; Milner-Brown and Penn, 1979; Sahrmann and Norton, 1977).        (2) Muscle strength: The individual is asked to exert force against an external resistance, usually the physicians hand. This test is useful to determine the distribution and extent of muscle weakness and paralysis. However, it is well known that both sensory and muscle control abnormalities contribute to weakness and paralysis.        (3) Conscious sense of limb position: The individual with eyes closed is asked to sense the position of a limb as it is passively moved. This method determines the extent of conscious position sense. In the control of posture and equilibrium, however, much of the useful sensory information does not reach consciousness (Nashner and Black, submitted). Thus, the conscious reports of subjects cannot be reliably used to determine the nature and extent of sensory impairment in the posture control system.        (4) Peripheral nerve conduction velocities: There are a number of electro-physiological tests for quantifying the speed of signal conduction within the peripheral motor and sensory nerves. These techniques can determine the distribution and extent of nerve damage contributing to an inability to contract muscle and sense the outcome of motor actions. Assessment of nerve conduction velocities is useful to rule out the possibility of peripheral nerve involvement. This technique, however, cannot separate and characterize sensory and motor impairment due to spinal cord and central brain disorders.        (5) Electromyograms (EMG): The recording of muscle electrical potentials using surface or in-dwelling needle electrodes can be used to identify peripheral neuropathies and number of disorders affecting muscle and muscle contractile mechanisms. Like peripheral nerve assessment, however, EMG's are useful to rule out peripheral causes but cannot separate and quantify the type and extent of sensory and motor impairment of central origin.        (6) Performance of motor tasks: To better characterize the distribution and nature of impaired posture and equilibrium functions, the physician typically observes the patient performing a number of simple motor tasks. Examples of such tasks include finger-to-nose movements, moving the heel of one foot up the shin of the opposite leg, performing rapid alternative rotations of the wrists, walking and performing rapid turns on command, standing and walking heel-to-toe, hopping on one foot, etc. Observations of this type, although valuable, are subjective and therefore cannot selectively assess individual sensory and motor components of posture and equilibrium.        
In addition to the standardized clinical assessment methods, devices have been developed to quantify measures human postural sway and postural movements. Several manufacturers currently produce fixed forceplate systems (Kistler Corporation, 75 John Glen Drive, Amherst, N. Y., 14120; Advanced Medical Technology, Inc., 141 California Street, Newton, Mass. 02158). These devices are used to measure the reaction forces exerted by the feed against the support surface. These measures are have been used by researchers and clinicians to quantify the spontaneous sway trajectories of subjects and patients with posture and movement disorders performing simple standing tasks (Arcan, et al, 1977; Baron, et al, 1975; Black, et al, 1978; Coats, 1973; Dietz, et al, 1980; Njiokiktjien and de Rijke, 1972; Japanese authors).